Abstract
We examined the possible roles of renal prostaglandins, renin-angiotensin and the kallikrein-kinin system in protein-induced glomerular hyperfiltration in normal subjects. The normal subjects were divided into three groups, i.e., control, indomethacin-treated and captopril-treated groups. Protein loading (0.6 g/kg BW as protein) resulted in a significant increase in glomerular filtration rate (GFR) from a baseline of 98 +/- 8 ml/min/1.73 M2 to 135 +/- 13 (P less than 0.01) in the control group. In both the indomethacin and captopril groups, significant elevations of GFR were observed after the test meal. The urinary kallikrein excretions after the meal were not significantly different from those for preloading in all groups. These results suggest that renal prostaglandins, renin-angiotensin and the kallikrein-kinin system may be less involved in protein-induced glomerular hyperfiltration in normal subjects.
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